The effects of CIL-102 on the prostate cancer cells

• Main Authors: Mong-Jun Yang, 楊孟俊
• Other Authors: Shu-Yu Li
• Format: Others
• Language: zh-TW
• Published: 2010
• Online Access: http://ndltd.ncl.edu.tw/handle/67148748158849799994

碩士 === 大仁科技大學 === 製藥科技研究所 === 98 === Hormone ablation so far remains the first-line treatment of prostate cancer. Hormone ablation therapy eventually fails for the most patients due to the diseases developing into hormone-refractory state. Thus, the U.S. (United State) Food and Drug Administration (FDA) have approved that docetaxel combined with prednisone can be utilized for the treatment of prostate cancers in this stage. The early result seems to show that patients can improve their chances of survival, suggesting that chemotherapy drugs with anti-microtubule capacity might be beneficial to hormone-refractory prostate cancer. Previous study has shown that CIL-102, claimed as a microtubule depolymerizer, leads PC3, a prostate cancer cell line, to arrest at G2-M, resulting in apoptosis eventually. In this study, we further analyzed CIL-102 effects on LNCaP cell, another prostate cancer cell line. The results indicated that CIL-102 also induces LNCaP cells to arrest at G2-M. However, we observed that treatment of LNCaP cells with CIL-102 causes multi-centrosomes with microtubule to associate with chromosome in random fashion, following by mitotic catastrophes. However, the treatment of PC3 cells with CIL-102 does not bring any abnormal distribution of microtubules. Actually CIL-102 can kill LNCaP or PC3 cells efficiently in vitro. Our results here raised a very interesting issue if CIL-102 might interact with same target existed in LNCaP and PC3 cells by the same mechanism, for example, by interacting with tubules. If so, LNCaP might possess a different machinery from PC3 for responding to this drug effect, vice versa.